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目的研究氯胺酮对局灶性脑缺血损伤大鼠脑N-甲基-D-天冬氨酸受体(NMDAR)-1 (NRⅠ)表达的影响。方法40只雄性SD大鼠,随机分为2组(n=20)：氯胺酮组和戊巴比妥组,分别腹腔注射氯胺酮60 mg·kg~(-1)或戊巴比妥40 mg·kg~(-1),翻正反向消失时,用线栓法阻塞大脑中动脉阻塞制备脑缺血模型。缺血24h时每组分别腹腔注射上述剂量的氯胺酮或戊巴比妥处死5只大鼠,测定脑梗塞体积,缺血24、72h分别腹腔注射上述剂量的氯胺酮或戊巴比妥处死4只大鼠,脑组织切片甲苯胺蓝染色后,观察半暗带内存活神经元情况,并行免疫组化染色,测定NR1表达水平。结果与戊巴比妥组比较,氯胺酮组大鼠脑梗塞体积减小,半暗带内神经元密度升高,NR1表达降低(P＜0.05)。结论氯胺酮抗大鼠脑缺血损伤的作用与下调NRⅠ表达有关。
Objective To investigate the effects of ketamine on the expression of N-methyl-D-aspartate receptor (NMDAR) -1 in rats with focal cerebral ischemia. Methods Forty male Sprague-Dawley rats were randomly divided into 2 groups (n = 20): ketamine group and pentobarbital group. The rats were given ketamine 60 mg · kg -1 or pentobarbital 40 mg · kg -1 ~ (-1), the right and reverse disappeared, occlusion of the middle cerebral artery occlusion by thread occlusion preparation of cerebral ischemia model. At 24 hours after ischemia, 5 rats in each group were killed by intraperitoneal injection of ketamine or pentobarbital at the above doses respectively. The volume of cerebral infarction was measured. After ischemia for 24 and 72 hours, ketamine or pentobarbital Rat and brain tissue sections were stained with toluidine blue to observe the survival neurons in the penumbra. Immunohistochemical staining was performed to determine the NR1 expression level. Results Compared with pentobarbital group, the volume of cerebral infarction in ketamine group was decreased, the density of neurons in penumbra was increased and the expression of NR1 was decreased (P <0.05). Conclusion The effect of ketamine on cerebral ischemia injury in rats is related to the downregulation of NR Ⅰ expression.